尝试纠正系统性红斑狼疮患者T淋巴细胞中异常的信号转导。

Attempt to correct abnormal signal transduction in T lymphocytes from systemic lupus erythematosus patients.

作者信息

Fujii Yuko, Fujii Koichi, Tanaka Yoshiya

机构信息

First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan.

出版信息

Autoimmun Rev. 2006 Feb;5(2):143-4. doi: 10.1016/j.autrev.2005.09.004. Epub 2005 Sep 19.

DOI:10.1016/j.autrev.2005.09.004

PMID:16431347

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease, which predominantly affects females, and causes multiple organ dysfunctions. Recent studies have revealed the underlying immunological abnormalities, especially in lymphocytes from SLE patients. T lymphocytes from SLE patients present abnormalities in T cell receptor (TCR) signaling, for example, decreased expression of TCR zeta chain, PKC theta, and NF-kB p65, decreased PKC dependent protein phosphorylation, impaired translocation of NF-kB p65, decreased production of IL-2 etc. Recently, it is known that reconstitution of deficient TCR zeta chain in T lymphocytes from SLE patients leads to restoration of impaired IL-2 production upon CD3/CD28 stimulation. This time, analysis of abnormal TCR signaling in SLE patients and attempt to correct the impaired IL-2 production by replenishing missing signaling molecules are to be discussed.

摘要

系统性红斑狼疮（SLE）是一种自身免疫性疾病，主要影响女性，并导致多器官功能障碍。最近的研究揭示了潜在的免疫异常，特别是在SLE患者的淋巴细胞中。SLE患者的T淋巴细胞在T细胞受体（TCR）信号传导方面存在异常，例如，TCR ζ链、蛋白激酶C θ（PKC θ）和核因子κB p65（NF-κB p65）的表达降低，PKC依赖性蛋白磷酸化减少，NF-κB p65的易位受损，白细胞介素-2（IL-2）的产生减少等。最近发现，在SLE患者的T淋巴细胞中重建缺陷的TCR ζ链可导致在CD3/CD28刺激后恢复受损的IL-2产生。此次，将讨论对SLE患者异常TCR信号传导的分析以及通过补充缺失的信号分子来纠正受损的IL-2产生的尝试。